Abstract

It has been demonstrated that periodontitis, a chronic oral disease, can induce systemic inflammation which is associated with systemic diseases, including rheumatoid arthritis. Here, we evaluated whether periodontitis can modulate the inflammatory response at a site distant to the oral cavity. Wistar rats were subjected to ligature-induced experimental periodontitis. Fourteen days after the procedure, paw edema was induced by carrageenan or by different receptor-specific inflammatory mediators. Blood and the tissue of the paws were obtained for TNF-α and IL-1β measurement. It was observed that carrageenan-induced paw edema and leukocyte migration was potentiated in periodontitis animals. The edema induced by carrageenan, bradykinin and des-Arg9-BK (B1 agonist) was also potentiated in periodontitis animals and blocked by a B1 antagonist. Ligature-induced periodontitis increased plasma levels of TNF-α and tissue IL-1β. Periodontitis also up-regulated kinin B1 receptor expression in paw tissue. Additionally, the treatment of ligature animals with anti-TNF-α, etanercept, completely abolished the potentiation of edema induced by des-Arg9-BK. Taken together, these results show that experimental periodontitis in rats can induce systemic inflammation through the up-regulation of kinin B1 receptors at a site distant from the oral cavity, modifying the inflammatory response.

Graphical abstract:

The experimental periodontitis in rats can induce systemic inflammation and up-regulate B1 receptors in the rat paw, modifying the inflammatory response at a site distant from oral infection.